scholarly journals White Adipose Tissue Depots Respond to Chronic Beta-3 Adrenergic Receptor Activation in a Sexually Dimorphic and Depot Divergent Manner

Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3453
Author(s):  
Eric D. Queathem ◽  
Rebecca J. Welly ◽  
Laura M. Clart ◽  
Candace C. Rowles ◽  
Hunter Timmons ◽  
...  
Keyword(s):  
Body Composition ◽  
Adipose Tissue ◽  
Glucose Tolerance ◽  
Protein Expression ◽  
Protein Content ◽  
White Adipose Tissue ◽  
Adrenergic Receptor ◽  
Receptor Activation ◽  
Control Male ◽  
Gene And Protein Expression

Beta-3 adrenergic receptor activation via exercise or CL316,243 (CL) induces white adipose tissue (WAT) browning, improves glucose tolerance, and reduces visceral adiposity. Our aim was to determine if sex or adipose tissue depot differences exist in response to CL. Daily CL injections were administered to diet-induced obese male and female mice for two weeks, creating four groups: male control, male CL, female control, and female CL. These groups were compared to determine the main and interaction effects of sex (S), CL treatment (T), and WAT depot (D). Glucose tolerance, body composition, and energy intake and expenditure were assessed, along with perigonadal (PGAT) and subcutaneous (SQAT) WAT gene and protein expression. CL consistently improved glucose tolerance and body composition. Female PGAT had greater protein expression of the mitochondrial uncoupling protein 1, while UCP1 (S, p < 0.001) was more responsive to CL in increasing UCP1 (S×T, p = 0.011) and the mitochondrial biogenesis induction protein, PPARγ coactivator 1α (PGC1α) (S×T, p = 0.026). Females also displayed greater mitochondrial OXPHOS (S, p < 0.05) and adiponectin protein content (S, p < 0.05). On the other hand, male SQAT was more responsive to CL in increasing protein levels of PGC1α (S×T, p = 0.046) and adiponectin (S, p < 0.05). In both depots and in both sexes, CL significantly increased estrogen receptor beta (ERβ) and glucose-related protein 75 (GRP75) protein content (T, p < 0.05). Thus, CL improves systemic and adipose tissue-specific metabolism in both sexes; however, sex differences exist in the WAT-specific effects of CL. Furthermore, across sexes and depots, CL affects estrogen signaling by upregulating ERβ.

scholarly journals Differential Patterns of Secreted Frizzled-Related Protein 4 (SFRP4) in Adipocyte Differentiation: Adipose Depot Specificity

2018 ◽  
Vol 46 (5) ◽  
pp. 2149-2164 ◽  
Author(s):  
Hua Guan ◽  
Yali Zhang ◽  
Shoucui Gao ◽  
Liang Bai ◽  
Sihai Zhao ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Protein Expression ◽  
Expression Analysis ◽  
White Adipose Tissue ◽  
Adipocyte Differentiation ◽  
Related Protein ◽  
Gene And Protein Expression ◽  
Significant Difference ◽  
Epididymal White Adipose Tissue ◽  
Visceral Adipose

Background/Aims: Secreted frizzled-related protein 4 (SFRP4) is a member of the SFRP family that acts as soluble modulators of Wnt signaling. Given the substantial rise in obesity, depot-specific fat accumulation and its associated diseases like diabetes, it is important to understand the molecular basis of depot-specific adipocyte differentiation. In the current study, we investigated the expression of SFRP4 in both subcutaneous and visceral adipose tissue in terms of their differentiation. Methods: White preadipocytes were isolated from the inguinal white adipose tissue (iWAT) and epididymal white adipose tissue (eWAT) from C57BL/6J mice (age: 8-week-old, male). SFRP4 expression in iWAT and eWAT preadipocytes was silenced by siRNA transfection and harvested cells for gene and protein expression analysis was performed during the differentiation. Furthermore, iWAT and eWAT preadipocytes treated with or without IL-1β were harvested for gene and protein expression analysis. Results: SFRP4 expression levels were gradually increased and proportionally associated with eWAT adipocyte differentiation toward maturation at 14 days, while iWAT adipocyte just showed an opposite tendency. Moreover, genetic (adiponectin, C/EBPα, C/EBPβ, FABP4, GLUT4 and PPARγ) analysis demonstrated that depot-specific adipogenesis in response to SFRP4 silencing in eWAT and iWAT preadipocytes. Upon IL-1β treatment, SFRP4 mRNA expression decreased significantly in iWAT adipocyte, but the expression was no significant difference in eWAT adipocyte. Conclusion: These results suggest that SFRP4 expression differentially mediates adipocyte differentiation and may play an important role in adipogenesis.

scholarly journals Emodin Improves Glucose and Lipid Metabolism Disorders in Obese Mice via Activating Brown Adipose Tissue and Inducing Browning of White Adipose Tissue

2021 ◽  
Vol 12 ◽  
Author(s):  
Long Cheng ◽  
Shuofeng Zhang ◽  
Fei Shang ◽  
Yibo Ning ◽  
Zhiqi Huang ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Glucose Tolerance ◽  
Protein Expression ◽  
Brown Adipose Tissue ◽  
White Adipose Tissue ◽  
Blood Lipids ◽  
The Body ◽  
Obese Mice ◽  
Brown Adipose

BackgroundAdipose tissue (e.g. white, brown and brite) plays a critical role in modulating energy metabolism. Activating brown adipose tissue (BAT) and inducing browning in white adipose tissue (WAT) has been proposed to be a potential molecular target for obesity treatment. Emodin is a natural anthraquinone derivative that exhibits variety of pharmacologic effects including lowering lipids and regulating glucose utilization. However, the underlying mechanism of action is still unclear. In the present study, we investigated whether emodin could alleviate obesity via promoting browning process in adipose tissue.MethodsC57BL/6J mice were fed with high fat diet to induce obesity. Emodin at the doses of 40 and 80 mg/kg were orally given to obesity mice for consecutive 6 weeks. Parameters including fasting blood glucose, oral glucose tolerance, blood lipids, and the ratios of subcutaneous white adipose tissue (scWAT) or BAT mass to body weight, and morphology of adipose tissue were observed. Besides, the protein expression of uncoupling protein 1 (UCP1) and prohibitin in BAT and scWAT was determined by immunohistochemistry method. Relative mRNA expression of Cd137, transmembrane protein 26 (Tmem26) and Tbx1 in scWAT was analyzed using qRT-PCR. And the protein expression of UCP1, CD36, fatty acid transporter 4 (FATP4), peroxisome proliferator-activated receptor alpha (PPARα) and prohibitin of scWAT and BAT were analyzed using western blotting. In addition, ultra-high-performance liquid chromatography with electrospray ionization tandem mass spectrometry was utilized to detect the small lipid metabolites of scWAT and BAT.ResultsEmodin decreased the body weight and food intake in HFD-induced obesity mice, and it also improved the glucose tolerance and reduced the blood lipids. Emodin treatment induced beiging of WAT, and more multilocular lipid droplets were found in scWAT. Also, emodin significantly increased markers of beige adipocytes, e.g. Cd137, Tmem26 and Tbx1 mRNA in scWAT, and UCP1, CD36, FATP4, PPARα and prohibitin protein expression in scWAT and BAT. Furthermore, emodin perturbed the lipidomic profiles in scWAT and BAT of obese mice. Emodin increased total ceramides (Cers), lysophosphatidylcholines (LPCs), lyso-phosphatidylcholines oxygen (LPCs-O), and phosphatidylethanolamines oxygen (PEs-O) species concentration in scWAT. Specifically, emodin significantly up-regulated levels of Cer (34:1), LPC (18:2), LPC-(O-20:2), PC (O-40:7), PE (O-36:3), PE (O-38:6), PE (O-40:6), and sphingolipid (41:0) [SM (41:0)], and down-regulated PC (O-38:0), PE (O-40:4), PE (O-40:5) in scWAT of obesity mice. In terms of lipid matabolites of BAT, the emodin remarkably increased the total PCs levels, which was driven by significant increase of PC (30:0), PC (32:1), PC (32:2), PC (33:4) and PC (38:0) species. In addition, it also increased species of LPCs, e.g. LPC (20:0), LPC (20:1), LPC (22:0), LPC (22:1), LPC (24:0), and LPC (24:1). Especially, emodin treatment could reverse the ratio of PC/PE in HFD-induced obese mice.ConclusionsThese results indicated that emodin could ameliorate adiposity and improve metabolic disorders in obese mice. Also, emodin could promote browning in scWAT and activate the BAT activities. In addition, emodin treatment-induced changes to the scWAT and BAT lipidome were highly specific to certain molecular lipid species, indicating that changes in tissue lipid content reflects selective remodeling in scWAT and BAT of both glycerophospholipids and sphingolipids in response to emodin treatment.

scholarly journals Identification of Nesfatin-1 in Human and Murine Adipose Tissue: A Novel Depot-Specific Adipokine with Increased Levels in Obesity

Endocrinology ◽  
2010 ◽  
Vol 151 (7) ◽  
pp. 3169-3180 ◽  
Author(s):  
Manjunath Ramanjaneya ◽  
Jing Chen ◽  
James E. Brown ◽  
Gyanendra Tripathi ◽  
Manfred Hallschmid ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Protein Expression ◽  
Food Deprivation ◽  
Inflammatory Cytokines ◽  
Energy Homeostasis ◽  
Culture Media ◽  
Nonesterified Fatty Acid ◽  
High Fat ◽  
Gene And Protein Expression ◽  
The Impact

Nesfatin-1 is a recently identified anorexigenic peptide derived from its precursor protein, nonesterified fatty acid/nucleobindin 2 (NUCB2). Although the hypothalamus is pivotal for the maintenance of energy homeostasis, adipose tissue plays an important role in the integration of metabolic activity and energy balance by communicating with peripheral organs and the brain via adipokines. Currently no data exist on nesfatin-1 expression, regulation, and secretion in adipose tissue. We therefore investigated NUCB2/nesfatin-1 gene and protein expression in human and murine adipose tissue depots. Additionally, the effects of insulin, dexamethasone, and inflammatory cytokines and the impact of food deprivation and obesity on nesfatin-1 expression were studied by quantitative RT-PCR and Western blotting. We present data showing NUCB2 mRNA (P &lt; 0.001), nesfatin-1 intracellular protein (P &lt; 0.001), and secretion (P &lt; 0.01) were significantly higher in sc adipose tissue compared with other depots. Also, nesfatin-1 protein expression was significantly increased in high-fat-fed mice (P &lt; 0.01) and reduced under food deprivation (P &lt; 0.01) compared with controls. Stimulation of sc adipose tissue explants with inflammatory cytokines (TNFα and IL-6), insulin, and dexamethasone resulted in a marked increase in intracellular nesfatin-1 levels. Furthermore, we present evidence that the secretion of nesfatin-1 into the culture media was dramatically increased during the differentiation of 3T3-L1 preadipocytes into adipocytes (P &lt; 0.001) and after treatments with TNF-α, IL-6, insulin, and dexamethasone (P &lt; 0.01). In addition, circulating nesfatin-1 levels were higher in high-fat-fed mice (P &lt; 0.05) and showed positive correlation with body mass index in human. We report that nesfatin-1 is a novel depot specific adipokine preferentially produced by sc tissue, with obesity- and food deprivation-regulated expression.

scholarly journals Impact of thermogenesis induced by chronic β3-adrenergic receptor agonist treatment on inflammatory and infectious response during bacteremia in mice

PLoS ONE ◽  
2021 ◽  
Vol 16 (8) ◽  
pp. e0256768
Author(s):  
Patrick Munro ◽  
Samah Rekima ◽  
Agnès Loubat ◽  
Christophe Duranton ◽  
Didier F. Pisani ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Adrenergic Receptor ◽  
Receptor Agonist ◽  
Acute Infection ◽  
Immunomodulatory Activity ◽  
Inflammatory Parameters ◽  
Brown Adipose ◽  
Thermogenic Adipocytes ◽  
Adrenergic Receptor Agonist

White adipocytes store energy differently than brown and brite adipocytes which dissipate energy under the form of heat. Studies have shown that adipocytes are able to respond to bacteria thanks to the presence of Toll-like receptors at their surface. Despite this, little is known about the involvement of each class of adipocytes in the infectious response. We treated mice for one week with a β3-adrenergic receptor agonist to induce activation of brown adipose tissue and brite adipocytes within white adipose tissue. Mice were then injected intraperitoneally with E. coli to generate acute infection. The metabolic, infectious and inflammatory parameters of the mice were analysed during 48 hours after infection. Our results shown that in response to bacteria, thermogenic activity promoted a discrete and local anti-inflammatory environment in white adipose tissue characterized by the increase of the IL-1RA secretion. More generally, activation of brown and brite adipocytes did not modify the host response to infection including no additive effect with fever and an equivalent bacteria clearance and inflammatory response. In conclusion, these results suggest an IL-1RA-mediated immunomodulatory activity of thermogenic adipocytes in response to acute bacterial infection and open a way to characterize their effect along more chronic infection as septicaemia.

Soybean and sunflower oil-induced insulin resistance correlates with impaired GLUT4 protein expression and translocation specifically in white adipose tissue

2010 ◽  
Vol 28 (2) ◽  
pp. 114-121 ◽  
Author(s):  
Ana Cláudia Poletto ◽  
Gabriel Forato Anhê ◽  
Paula Eichler ◽  
Hilton Kenji Takahashi ◽  
Daniela Tomie Furuya ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Protein Expression ◽  
White Adipose Tissue ◽  
Sunflower Oil

Meprin-α in chronic diabetic nephropathy: interaction with the renin-angiotensin axis

2005 ◽  
Vol 289 (4) ◽  
pp. F911-F921 ◽  
Author(s):  
Roy Mathew ◽  
Stephen Futterweit ◽  
Elsa Valderrama ◽  
Antonio A. Tarectecan ◽  
John E. Bylander ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Kidney Disease ◽  
Protein Expression ◽  
Protein Content ◽  
Ace Inhibitor ◽  
Inhibitor Therapy ◽  
Treated Water ◽  
Renin Angiotensin ◽  
Gene And Protein Expression ◽  
The Impact

Meprin (MEP) A is a metalloendopeptidase that is present in the renal proximal tubule brush-border membrane (BBM) and that colocalizes with angiotensin-converting enzyme (ACE). The MEP β-chain gene locus on chromosome 18 has been linked to a heightened risk of diabetic nephropathy (DN) in patients with type 2 diabetes. This study evaluated 1) whether MEP-α and MEP-β gene and protein expression are altered in db/db mice before the onset of DN and 2) the role of MEP-α in the pathogenesis of DN and the impact of the renin-angiotensin system on this interaction in two experimental models of diabetes. MEP-α and MEP-β gene and protein expression were evaluated in db/db mice, 13–14 wk of age, compared with lean C57BLKS/J littermate animals. A treatment study was then performed in which db/db mice and controls were assigned to one of three groups: control (C) water, no therapy; ACE inhibitor therapy, enalapril (EN)-treated water, 50 mg/l; ANG II receptor type 1 blocker (ARB) therapy, losartan (LOS)-treated water, 500 mg/l. Treatment was started at 8 wk of age and continued for 52 wk. Male Sprague-Dawley rats with diabetes for 52 wk following a single dose of streptozocin (STZ; 60 mg/kg) were also studied. At 13.5 wk of age, MEP-α and MEP-β kidney mRNA abundance and protein expression were significantly lower in db/db mice compared with lean controls, with greater changes in MEP-β ( P < 0.05). In the treatment study, EN ameliorated and LOS exacerbated DN in db/db mice. BBM MEP A enzymatic activity and MEP-α protein content were lower in db/db mice vs. control nonobese mice at 52 wk ( P < 0.02). EN-treated db/db mice showed increased MEP A activity, MEP-α content in BBM, decreased urinary MEP-α excretion, and enhanced BBM staining for MEP-α protein vs. C and LOS-treated db/db mice. In nonobese mice, EN and LOS treatment had no effect on MEP-α expression. In rats with STZ-induced diabetes for 52 wk, urinary MEP-α excretion was increased and MEP A activity and MEP-α protein content per milligram of BBM protein were decreased compared with age-matched control animals ( P < 0.05). These results indicate that db/db mice manifest decreased MEP-α and MEP-β gene and protein expression, before the development of overt kidney disease. Moreover, in db/db mice with DN and rats with STZ-diabetes, there was an inverse relationship between renal MEP-α content and the severity of the renal injury. Treatment with an ACE inhibitor was more effective than ARB in ameliorating DN in db/db mice, a change that correlated with alterations in urinary excretion and BBM content of MEP-α. MEP-α may play a role in the pathogenesis of DN and the benefits of ACE inhibitor therapy on the progression of diabetic kidney disease may be related, in part, to its impact on renal MEP-α expression.

scholarly journals Lipases and lipid droplet-associated protein expression in subcutaneous white adipose tissue of cachectic patients with cancer

2017 ◽  
Vol 16 (1) ◽  
Author(s):  
Renata Silvério ◽  
Fábio S. Lira ◽  
Lila M. Oyama ◽  
Cláudia M. Oller do Nascimento ◽  
José P. Otoch ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Protein Expression ◽  
Lipid Droplet ◽  
White Adipose Tissue ◽  
Subcutaneous White Adipose Tissue ◽  
Patients With Cancer
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